Fibromyalgia and the Immune System: Emerging Evidence and Advances

Fibromyalgia syndrome (FMS) is a chronic debilitating pain disorder that affects at least 4% of the global population. Despite its prevalence, the biological underpinnings of FMS remain incompletely understood, leaving patients with limited diagnostic tools and few effective, mechanism-based treatments. Over the last decade, however, advances in basic and translational science have provided remarkable new insights into immune-mediated processes that may contribute directly to the pathophysiology of FMS.
This workshop will focus on emerging cellular and molecular mechanisms that highlight the role of immune function in shaping disease expression, patient heterogeneity, and symptom persistence. By bringing together recent discoveries from immunology, neuroscience, and clinical pain research, we will explore how these findings can inform the development of future biomarkers and targeted therapeutic strategies.
The discussion will be anchored by three complementary themes:
• Neutrophil dysfunction in fibromyalgia — examining altered neutrophil reactivity and impaired NF-κB regulation as contributors to patient heterogeneity and highlighting how neutrophils and their signaling pathways may directly sensitize neurons and amplify pain in FMS.
• Autoimmune mechanisms in fibromyalgia — presenting new evidence that anti-satellite glial cell (anti-SGC) IgGs contribute to immune, and pain-related mechanisms of FMS, linking autoantibody activity of the patients’ serum to the clinical manifestations of FMS.
• Development of novel preclinical models — exploring innovative approaches to model fibromyalgia in mice through the transfer of patient-derived biological material. Specifically, models based on transfer of plasma, IgG and neutrophils. Together, these new strategies provide powerful back-translational tools to define the neuro-immune basis of symptom generation and potential therapeutic strategies.

By linking these discoveries to their potential clinical applications, this session will bridge the gap between basic mechanistic science and clinical outcomes in FMS. Attendees will gain an integrated understanding of how immune-related findings are reshaping the field’s conceptual framework of FMS and how these insights may ultimately lead to improved diagnostic stratification and novel, mechanism-based treatment approaches.
At this workshop, attendees will:
• Become familiar with emerging evidence for the role of neutrophil dysfunction and NF-κB regulation in shaping FMS heterogeneity.
• Understand how anti-SGC IgGs may mediate autoimmune contributions to immune activation, neuronal sensitization, and pain symptoms.
• Learn about the development and applications of a novel plasma-transfer mouse model of fibromyalgia as a translational research platform.